Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, NSW Australia.
Med Sci Sports Exerc. 2010 Feb;42(2):273-80. doi: 10.1249/MSS.0b013e3181b541b1.
The aim of this study was to assess whether a single high dose of beclomethasone dipropionate (BDP) could blunt mast cell activation and bronchoconstriction after eucapnic voluntary hyperpnea (EVH).
In this model of exercise-induced bronchoconstriction (EIB), seven athletes with EIB and eight untrained subjects with mild asthma performed two EVH tests 5.5 h apart on the same day; the first challenge after inhalation of a placebo aerosol and the second 4 h after inhalation of BDP (1500 microg). Prechallenge and postchallenge pulmonary function and urinary excretion of the mast cell mediator 9alpha, 11beta-prostaglandin (PG) F2 were followed, as well as urinary excretion of the bronchoconstrictor leukotriene (LT) E4.
The EVH-induced bronchoconstriction was inhibited by BDP in both groups (P < 0.001): in athletes, mean +/- SEM percent fall in forced expiratory volume in 1 s was 22% +/- 4% after placebo versus 13% +/- 3% after BDP; in subjects with asthma, 23% +/- 4% after placebo versus 14 +/- 3% after BDP. This inhibition of airway response was associated with a significant reduction in the urinary excretion of 9alpha,11beta-PGF2 (P = 0.039) and LTE4 (P = 0.003) in both groups. Significant correlations were found between the percent fall in forced expiratory volume in 1 s and the increase in urinary excretion of both mediators 9alpha,11beta-PGF2 (r = 0.544, P = 0.002) and LTE4 (r = 0.380, P = 0.038) after EVH.
We conclude that a single dose of BDP has an acute protective effect on the bronchial response to hyperpnea in both untrained subjects with asthma and athletes with EIB. This effect was associated with decreased excretion of urinary mediators, suggesting that BDP blunted the mast cell activation.
本研究旨在评估丙酸倍氯米松（BDP）单次高剂量给药是否可抑制运动诱发支气管痉挛（EIB）患者的气道平滑肌收缩和肥大细胞激活。
在该模型中，7 名 EIB 运动员和 8 名轻度哮喘的非训练对照者在同一天进行了 2 次呼入安慰剂和 BDP（1500μg）后的 Eucapnic 自愿性 Hyperpnea（EVH）测试；首次激发后 5.5 小时和第二次激发后 4 小时进行肺功能和尿中 9α，11β-前列腺素（PG）F2 检测，同时检测尿中白三烯（LT）E4 的排泄。
BDP 可抑制 EVH 诱导的支气管收缩，在两组中均有统计学差异（P<0.001）：运动员组中，吸入安慰剂后，FEV1 下降 22%±4%，而吸入 BDP 后，FEV1 下降 13%±3%；在哮喘对照组中，FEV1 下降 23%±4%，而吸入 BDP 后，FEV1 下降 14%±3%。气道反应的抑制与尿中 9α，11β-PGF2（P=0.039）和 LTE4（P=0.003）排泄的显著减少相关。在两组中，FEV1 下降百分比与两种介质尿中排泄的增加之间存在显著相关性：9α，11β-PGF2（r=0.544，P=0.002）和 LTE4（r=0.380，P=0.038）。
我们得出结论，BDP 单次剂量给药对未经训练的哮喘患者和 EIB 运动员的 Hyperpnea 支气管反应具有急性保护作用。这种作用与尿中介质排泄减少有关，表明 BDP 抑制了肥大细胞的激活。
